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Understanding the clinical picture key to effective IB control

By Mark W. Jackwood Poultry Diagnostic and Research Center University of Georgia Athens, Ga.

Avian infectious bronchitis virus (IBV) is a highly contagious coronavirus found in chickens worldwide that costs the US poultry industry millions of dollars annually. Although it’s largely a respiratory disease, some strains of the virus can also cause kidney lesions resulting in nephritis, and in hens, the virus can replicate in the reproductive tract causing egg quality and production losses.

Serotype = different virus types defined by antisera able to neutralize the virus.Genetic type = different virus types characterized by the genetic sequence of their spike gene.

IBV exists in the field as many different types, defined as serotypes or genetic types (see box). In addition, the term “variant” is often used to describe a newly identified but not yet characterized type of the virus.

Currently, the best strategy for managing the disease is the use of modified live IBV vaccines. However, because different serotypes or genetic types of IBV don’t cross-protect, the disease is very difficult to control. Selection of appropriate vaccines requires knowledge about the virus type that’s causing disease in the field.

Compounding this situation is the ability of IBV — like most RNA viruses — to rapidly change and adapt to the host when they replicate. This can result in the emergence of new virus types that cause disease even in vaccinated birds. This underscores the importance of selecting an appropriate vaccine so that virus replication can be significantly reduced.

Sometimes, however, there’s no combination of vaccine serotypes that will provide adequate cross-protection, especially once an emerging IBV has reached a critical mass.

The clinical picture

Clinical signs associated with an IBV respiratory tract infection include watery eyes, mucus in the naris and trachea, and tracheal rales. Decreased weight gain and feed efficiency as well as open-mouth breathing, swollen sinuses and lethargy are also among the common signs observed.

Birds in lay can experience drops in egg production and misshapen eggs; brown eggs can become pale and the albumen watery. Strains of IBV that affect the kidney can result in diarrhea, severe dehydration and mortality due to kidney failure.

The disease starts as a respiratory tract infection and then goes systemic, infecting other organs including the reproductive tract and kidney. In addition, the immune response carries the virus to the cecal tonsils where it can be found for several weeks after the initial infection.

There are many factors that can affect the severity of IBV disease and, thus, the clinical signs observed. These include the virulence of the virus, the age and sex of the bird, the type of bird, the bird’s immune status and stressful environmental conditions.

Factors affecting severity of the disease

Strain differences. There are approximately 70 different strains of IBV circulating in commercial poultry worldwide,1 and those strains have varying types of pathogenicity and degrees of virulence. The strain’s degree of virulence can lead to a wide variety of respiratory signs ranging from very mild, consisting only of watery eyes and some mucus in the nares, to severe with extensive mucus production in the trachea resulting in tracheal rales.

Likewise, some strains will cause only a slight drop in egg quality and production in hens, whereas highly virulent strains can cause severe egg losses as high as 70% or more.

Pathogenicity = the ability to cause a specific disease. A virus is either pathogenic or not.Virulence = the severity of the disease. The disease caused by pathogenic viruses can be mild, moderate or severe.

In addition, different IBV strains can cause distinctive egg quality problems including variations in pigment, thinning of shells and watery albumen.

Lesions in the kidney caused by nephropathogenic strains of IBV are almost always severe because even slight kidney damage can result in watery diarrhea, dehydration and mortality.

Based on characterization in the laboratory, some examples of highly virulent IBV strains include Arkansas, Australia T and QX, among others. Mild strains include Connecticut, some strains of Massachusetts and some California strains such as CA/1737/04.

Viral load. The amount of virus in the bird, or viral load, is directly related to the efficiency of virus replication. A high viral load allows IBVs to be easily transmitted from one bird to the next, which is a major factor in the emergence of certain IBV types. Viral load can help explain how new variants seem to emerge unexpectedly and why IBV is mostly a winter/spring disease in the U.S — there’s less dilution of IBVs with decreased ventilation. Air quality and environmental stress are obviously factors, but viral load plays a big role too. Longer, colder winters provide more opportunity for IBVs to replicate, cause outbreaks and spread.

Age of the bird. The age of the bird when infected with IBV affects the clinical outcome of the disease. In general, respiratory signs tend to be more severe in younger birds. In addition, infection of breeder chicks can result in damage to the immature reproductive tract, leading to false layers.

Higher mortality may be associated with infection in chicks compared to older birds, particularly with nephropathogenic IBV strains, and young hens recently brought into production can experience more dramatic egg-quality and production losses compared to older layers.

Males and females. The sex of the bird can affect the severity of the clinical signs associated with IBV. Males appear to be more susceptible than females, but we don’t know why.

Type of chicken affected. It’s well known that broilers have more severe respiratory signs when infected with IBV compared to layer-type birds. However, different breeds of layers and broilers can be more or less susceptible. It has been shown that birds with a B12, B15 or B19 genetic makeup (major histocompatibility type or B haplotype) are more resistant to the disease than birds with B2, B5, B13 or B21 haplotypes. Haplotypes are groups of inherited genes.

Immunity. The immune status of the bird can significantly affect the clinical outcome of IBV infection. Maternally derived antibodies can help protect chicks for up to 2 weeks, depending on the level of antibodies in the chicks. Active immunity that results after administration of appropriate vaccines can protect birds from clinical signs, whereas infections in immune-suppressed birds can result in severe clinical signs.

Environment. Poor environmental conditions in the chicken house can contribute to the severity of the clinical picture associated with IBV infection. High ammonia levels have been shown to cause ciliostasis, possibly resulting in more severe disease when they occur at the time of infection.

Of course, any environmental conditions that cause significant stress to the bird can result in a more severe clinical picture. These conditions include a temperature that’s too high or low, poor air quality due to dust and ammonia, overcrowding, wet litter, poor feed quality or feed restriction, and poor water quality and supply. In addition, co-infections with other respiratory disease agents such as Newcastle disease virus, infectious laryngotracheitis virus, avian influenza virus and avian mycoplasmas, and secondary, opportunistic bacterial infections such as Escherichia coli can significantly contribute to the severity of the IBV clinical signs observed and to resulting production losses and mortality. Opportunistic Escherichia coli infections can also lead to increased condemnations due to airsacculitis, pericarditis and perihepatitis.

Summary

The severity of the disease caused by IBV can be affected by many factors including strain of the virus, age of the bird, sex, genetic haplotype, immune status and chicken-house environmental factors. The virus typically causes lesions in the upper respiratory tract, but the reproductive tract and kidney can also be affected.

In addition, co-infections and opportunistic pathogens can compound the disease situation, which often significantly increases the severity of the disease. It’s important to remember that these variables alone or in combination can contribute to the nature and severity of the clinical picture observed for IBV infections in the field.

An in-depth review of IBV that I co-authored with IBV expert Sajak de Wit, DVM, PhD, EVSPVS, immunologist and poultry veterinarian at GD Animal Health Services, Deventer, The Netherlands, can be found in Diseases of Poultry, 13th edition, published by John Wiley and Sons.

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